title: A pilot study examining the relationship among Crohn disease activity, glucagon-like peptide-2 signalling and intestinal function in pediatric patients.
abstract: BACKGROUND⁄
  
  
  OBJECTIVE
  The relationship between the enteroendocrine hormone glucagon-like peptide 2 (GLP-2) and intestinal inflammation is unclear. GLP-2 promotes mucosal growth, decreases permeability and reduces inflammation in the intestine; physiological stimulation of GLP-2 release is triggered by nutrient contact. The authors hypothesized that ileal Crohn disease (CD) affects GLP-2 release.
  
  
  METHODS
  With ethics board approval, pediatric patients hospitalized with CD were studied; controls were recruited from local schools. Inclusion criteria were endoscopy-confirmed CD (primarily of the small intestine) with a disease activity index >150. Fasting and postprandial GLP-2 levels and quantitative urinary recovery of orally administered 3-O-methyl-glucose (active transport) and lactulose⁄mannitol (passive) were quantified during the acute and remission phases.
  
  
  RESULTS
  Seven patients (mean [± SD] age 15.3 ± 1.3 years) and 10 controls (10.3 ± 1.6 years) were studied. In patients with active disease, fasting levels of GLP-2 remained stable but postprandial levels were reduced. Patients with active disease exhibited reduced glucose absorption and increased lactulose⁄mannitol recovery; all normalized with disease remission. The change in the lactulose⁄mannitol ratio was due to both reduced lactulose and increased mannitol absorption.
  
  
  CONCLUSIONS
  These findings suggest that pediatric patients with acute ileal CD have decreased postprandial GLP-2 release, reduced glucose absorption and increased intestinal permeability. Healing of CD resulted in normalization of postprandial GLP-2 release and mucosal functioning (nutrient absorption and permeability), the latter due to an increase in mucosal surface area. These findings have implications for the use of GLP-2 and feeding strategies as a therapy in CD patients; further studies of the effects of inflammation and the GLP-2 axis are recommended.
authors.forename: David L
authors.initials: DL
authors.lastname: Sigalet
authors.forename: Dragan
authors.initials: D
authors.lastname: Kravarusic
authors.forename: Decker
authors.initials: D
authors.lastname: Butzner
authors.forename: Bolette
authors.initials: B
authors.lastname: Hartmann
authors.forename: Jens J
authors.initials: JJ
authors.lastname: Holst
authors.forename: Jon
authors.initials: J
authors.lastname: Meddings
mesh_terms: D019325:3-O-Methylglucose / Q000652:urine; D000293:Adolescent; D002648:Child; D003424:Crohn Disease / Q000503:physiopathology*; D005260:Female; D053767:Glucagon-Like Peptide 2 / Q000097:blood*; D006801:Humans; D007408:Intestinal Absorption; D007421:Intestine, Small / Q000378:metabolism*; D007792:Lactulose / Q000652:urine; D008137:Longitudinal Studies; D008297:Male; D008353:Mannitol / Q000652:urine; D010865:Pilot Projects; D019518:Postprandial Period; D015398:Signal Transduction / Q000502:physiology
chemical_list: D053767:Glucagon-Like Peptide 2; D019325:3-O-Methylglucose; D008353:Mannitol; D007792:Lactulose